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December 4, 2024 60 mins

Several years ago, a medical case appeared that took the scientific and medical community by storm. A patient appeared for surgery who reported never feeling anxiety, depression, or pain, despite numerous injuries and surgeries for which she required treatment.  As scientists analyzed her genetic profile, they discovered something amazing - Joanne Cameron lacked the genetic code that was responsible for transmitting pain and creating anxiety and depression.

In this episode of Cannabis Nurse Truths, we examine the curious case of Joanne Cameron that has led to some very surprising research that targets this important physiological phenomenon, and drug companies are furiously developing drugs to capitalize on this incredible potential to decrease pain, anxiety, depression, and treat a number of psychological and physical disorders. One of the most incredible findings linked to this case: cannabinoids, like CBD, also enhance the natural physiological activities of the body linked to the FAAH-OUT gene, where inflammation is halted (reducing pain), while also reducing or eliminating anxiety and depression.  

 

EPISODE RESOURCES

Ahn, K., Johnson, D. S., & Cravatt, B. F. (2009). Fatty acid amide hydrolase as a potential therapeutic target for the treatment of pain and CNS disorders. Expert Opinion on Drug Discovery, 4(7), 763–784. https://pmc.ncbi.nlm.nih.gov/articles/PMC2882713/pdf/nihms-116402.pdf  

Bartel, S. J., Sherry, S. B., & Stewart, S. H. (2020). Self-isolation: A significant contributor to cannabis use during the COVID-19 pandemic. Substance Abuse, 41(4), 409–412. https://pubmed.ncbi.nlm.nih.gov/33044893/ 

Bisogno, T., & Maccarrone, M. (2013). Latest advances in the discovery of fatty acid amide hydrolase inhibitors. Expert Opinion on Drug Discovery. https://www.researchgate.net/publication/236044861_Latest_advances_in_the_discovery_of_fatty_acid_amide_hydrolase_inhibitors 

Boileau, I., Mansouri, E., Williams, B., Le Foll, B., Rusjan, P., Mizrahi, R., Tyndale, R. F., Huestis, M. A., Payer, D. E., Wilson, A. A., Houle, S., Kish, S. J., & Tong, J. (2016). Fatty acid amide hydrolase binding in brain of cannabis users: Imaging with the novel radiotracer [11C]CURB. Biological Psychiatry, 80(9), 691–701. https://pubmed.ncbi.nlm.nih.gov/27345297/  

Bornscheuer, L., Lundin, A., Forsell, Y., Lavebratt, C., & Melas, P. A. (2023). Functional variation in the FAAH gene is directly associated with subjective well-being and indirectly associated with problematic alcohol use. Genes, 14(9), 1826. https://pubmed.ncbi.nlm.nih.gov/37761966/ 

Cravatt, B.F., & Lichtman, A.H. (2003). Fatty acid amide hydrolase: An emerging therapeutic target in the endocannabinoid system. Current Opinion in Chemical Biology, 7(4), 469–475. https://pubmed.ncbi.nlm.nih.gov/12941421/ 

Di Marzo, V., & Petrosino, S. (2007). Endocannabinoids and the regulation of their levels in health and disease. Current Opinion in Lipidology, 18(2), 129–140. https://pubmed.ncbi.nlm.nih.gov/17353660/ 

D’Souza, D. C., Cortes-Briones, J., Creatura, G., Bluez, G., Thurnauer, H., Deaso, E., Bielen, K., Surti, T., Radhakrishnan, R., Gupta, A., Gupta, S., Cahill, J., Sherif, M. A., Makriyannis, A., Morgan, P. T., Ranganathan, M., & Skosnik, P. D. (2019). Efficacy and safety of a fatty acid amide hydrolase inhibitor (PF-04457845) in the treatment of cannabis withdrawal and dependence in men: A double-blind, placebo-controlled, parallel group, phase 2a single-site randomised controlled trial. Lancet Psychiatry, 6(1), 35–45. https://www.thelancet.com/journals/lanpsy/article/PIIS2215-0366(18)30427-9/abstract 

Girella, A., Di Bartolomeo, M., Dainese, E., Buzzelli, V., Trezza, V., & D’Addario, C. (2024). Fatty acid amide hydrolase and cannabinoid receptor type 1 genes regulation is modulated by social isolation in rats. Neurochemical Research, 49(5),1278-1290. http://www.ncbi.nlm.nih.gov/pubmed/38368587 

Giuffrida, A., Leweke, F. M., Gerth, C. W., Schreiber, D., Koethe, D., Faulhaber, J., Klosterkötter, J., & Piomelli, D. (2004). Cerebrospinal anandamide levels are elevated in acute schizophrenia and are inversely correlated with psychotic symptoms. Neuropsychopharmacology, 29(11), 2108–2114.


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